Iron-chelating and anti-lipid peroxidation properties of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) in long-term iron loading β-thalassemic mice
10.12980/APJTB.4.2014APJTB-2014-0155
- Author:
Kanokwan KULPRACHAKARN
1
;
Nittaya CHANSIW
1
;
Somdet SRICHAIRATANAKOOL
1
;
Kanjana PANGJIT
2
;
Chada PHISALAPHONG
3
;
Suthat FUCHAROEN
4
;
Robert C. HIDER
5
;
Sineenart SANTITHERAKUL
6
Author Information
1. Department of Biochemistry, Faculty of Medicine, Chiang Mai University
2. College of Medicine and Public Health, Ubon Ratchathani University
3. Institute of Research and Development, Government Pharmaceuticals Organization, Ministry of Public Health
4. Thalassemia Research Center, Institute of Molecular Biosciences, Mahidol University Salaya Campus
5. Institute of Pharmaceutical Science, King's College London
6. Medical Science Research Equipment Center, Faculty of Medicine, Chiang Mai University
- Publication Type:Journal Article
- Keywords:
Iron chelator;
Iron overload;
Iron-chelating;
Lipid peroxidation;
Non-transferrin bound iron;
β-thalassemia
- From:Asian Pacific Journal of Tropical Biomedicine
2014;4(8):663-668
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To evaluate the iron-chelating properties and free-radical scavenging activities of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) treatment in chronic iron-loaded β-thalassemic (BKO) mice. Methods: The BKO mice were fed with a ferrocene-rich diet and were orally administered with CM1 [50 mg/(kg.day)] for 6 months. Blood levels of non-transferrin bound iron, labile plasma iron, ferritin (Ft) and malondialdehyde were determined. Results: The BKO mice were fed with an iron diet for 8 months which resulted in iron overload. Interestingly, the mice showed a decrease in the non-transferrin bound iron, labile plasma iron and malondialdehyde levels, but not the Ft levels after continuous CM1 treatment. Conclusions: CM1 could be an effective oral iron chelator that can reduce iron overload and lipid peroxidation in chronic iron overload β-thalassemic mice.